証拠の内容は英語で管理されます。

ひと目でわかる

ENTRY TYPE
research market
IDENTITY
Sequence verified

No structure asset recorded

TOP EVIDENCE
Grade D — Anabolic (rodent)
MAJOR STATUS
Jurisdiction-specific — see status table
SPORT
Prohibited — as of 2026-08-06
VERIFIED
2026-08-06

Bottom line

Des(1-3) IGF-1 is a truncated variant of human IGF-1 lacking the N-terminal tripeptide Gly-Pro-Glu (residues 1-3), resulting in a 67-amino-acid peptide. The truncation removes a key IGFBP-binding domain, reducing sequestration by IGF-binding proteins and thereby increasing free peptide available to activate the IGF-1 receptor. In cell assays it is approximately 7–10 times more potent than native IGF-1, and in rodent models approximately 2.5 times more potent. However, this enhanced potency reflects reduced IGFBP binding, not stronger receptor affinity. There are no controlled human trials; the entire evidence base is .

Identity and composition

FieldVerified information
Preferred nameDes(1-3) IGF-1
Key aliasesIGF-1 DES, destripeptide IGF-1, Delta-3 IGF-1, truncated IGF-1
Molecular/sequence identity67-amino-acid truncated version of human IGF-1; sequence same as native IGF-1(4-70)
Modifications/formRemoval of N-terminal Gly-Pro-Glu tripeptide; three disulfide bonds
Stable identifiersCAS: 112603-35-7; MW ~7365 Da
Identity caveatsNot mecasermin. Des(1-3) IGF-1 is explicitly distinct from the FDA-approved drug mecasermin (full-length rhIGF-1). The approval of mecasermin does not apply to this truncated variant. The enhanced potency is an availability effect, not stronger receptor binding.

Development and approval status

JurisdictionStatus and indicationProduct/sourceAs of
US (FDA)No regulatory status; research use only2026-08-06
Registers reviewedNo FDA-approved product or EMA-authorized medicine identified; status elsewhere requires a current national-register check2026-08-06
Status is multi-axis
Des(1-3) IGF-1 authorization and sport-status profileFour medicine-authorization axes reproduce only documented status rows; sport status is shown separately.UNITED STATESNo regulatory status; researchuse onlySOURCE / AS OFROW 1 / 2026-08-06EU/EEASOURCE ROW OMITTEDSEE AUDIT REASONSOURCE / AS OFNOT PRESENT / NOT RECORDEDUNITED KINGDOMSOURCE ROW OMITTEDSEE AUDIT REASONSOURCE / AS OFNOT PRESENT / NOT RECORDEDOTHER DOCUMENTEDNo FDA-approved product orEMA-authorized medicineSOURCE / AS OFROW 2 / 2026-08-06SPORT STATUS — SEPARATE FROM MEDICINE AUTHORIZATIONDes(1-3) IGF-1 is an IGF-1 analog and falls within WADA S2 prohibition. No authorized humanmedicinal product was identified in the jurisdictions and regulator databases reviewed; that
Authorization belongs to the named product, use, place, and date; sport status is independent.
テキストによる説明
UNITED STATES
US (FDA): No regulatory status; research use only
EU/EEA
No EU/EEA row is present in the source status table
UNITED KINGDOM
No UNITED KINGDOM row is present in the source status table
OTHER DOCUMENTED
Registers reviewed: No FDA-approved product or EMA-authorized medicine identified; status elsewhere requires a current national-register check

Sport status: Des(1-3) IGF-1 is an IGF-1 analog and falls within WADA S2 prohibition. No authorized human medicinal product was identified in the jurisdictions and regulator databases reviewed; that finding is not a universal legal opinion.

Mechanism and pharmacology

Des(1-3) IGF-1 binds the IGF-1 receptor with comparable or slightly reduced affinity compared to native IGF-1. Its enhanced potency arises from dramatically reduced affinity for IGFBPs (especially IGFBP-3), which normally sequester >95% of circulating IGF-1. By evading IGFBP binding, a greater proportion remains in the free, bioactive form. This is an availability effect, not a super-agonist mechanism. The peptide was first identified in bovine colostrum and human brain tissue as a naturally occurring truncated form.

Evidence by claim

Claim/indicationStageGradeBest human evidenceMain resultImportant limitations
Anabolic (rodent) [1]DLemmey et al., Am J Physiol 1991; rat gut resection modelIncreased weight gain, nitrogen retention, muscle protein synthesis vs IGF-1Animal only; no human data
Cell proliferation (in vitro)Preclinical?Ballard et al., multiple 1990s in vitro studies7-10× potency vs native IGF-1 in cell bioassaysIn vitro only; does not predict human in vivo effects
Human therapeutic useNoneXNo human studiesNo evidenceNo human safety or efficacy data exist
エビデンスグレード
  • AグレードA: 特定の表示使用に対して確立
  • BグレードB: 中等度のヒトエビデンス
  • CグレードC: 予備的ヒトエビデンス
  • DグレードD: 前臨床のみ
  • EグレードE: 逸話的/マーケティング主張
  • XグレードX: エビデンスが主張と矛盾するか、支持しない
エビデンスグレーディングの詳細
Claim-evidence profile
Des(1-3) IGF-1 claim-evidence profileA: 0 claims; B: 0 claims; C: 0 claims; D: 1 claim; E: 0 claims; X: 1 claimCONTRADICTORY / NON-SUPPORTIVEA — Established for a specific labeled useGrade A: Established for a specific labeled use — current approval plus adequate controlled trials and post-market context.0 claimsB — Moderate human evidenceGrade B: Moderate human evidence — multiple controlled studies or a strong pivotal study, but no current approval for the claim.0 claimsC — Preliminary human evidenceGrade C: Preliminary human evidence — small, uncontrolled, surrogate-endpoint, or early-phase studies.0 claimsD — Preclinical onlyGrade D: Preclinical only — in vitro or animal evidence with no adequate human efficacy evidence.1 claimAnabolic (rodent)E — Anecdotal/marketing claimGrade E: Anecdotal/marketing claim — testimonials, extrapolation, or vendor claims without adequate scientific support.0 claimsX — Evidence contradicts or does not support the claimGrade X: Evidence contradicts or does not support the claim — adequate negative evidence, failed program, or claim inconsistent with the studied material.1 claimHuman therapeutic use
This counts the page's claim rows; it does not average them into a score.
テキストによる説明

Text alternative for the claim-evidence diagram. Each grade is defined below:

AEstablished for a specific labeled use
0 claims
BModerate human evidence
0 claims
CPreliminary human evidence
0 claims
DPreclinical only
1 claim: Anabolic (rodent)
EAnecdotal/marketing claim
0 claims
XEvidence contradicts or does not support the claim
1 claim: Human therapeutic use
United StatesNo regulatory status; research use only
OtherNo FDA-approved product or EMA-authorized medicine identified; status elsewhere requires a current national-register check

Key studies

StudyDesign/populationExposure studiedEndpoints and resultLimitations
Lemmey et al., Am J Physiol 1991; PMID: 1996625Rat gut resection model [1] infusion, 0.96 mg/kg/dayIncreased weight gain and nitrogen retention; ~2.5× potency vs native IGF-1Rodent model; acute exposure only
Ballard et al., Prog Growth Factor Res 1991Cell-based bioassaysIn vitro7-10× increased potency vs native IGF-1In vitro; does not predict in vivo human response
Francis et al., J Mol Endocrinol 1992Structural characterizationIn vitroReduced IGFBP binding confirmed characterization only

Dose and administration evidence

Approved labeled regimen

Not applicable.

Studied regimens (not recommendations)

No established or recommended human dose. In rodent studies, ~1–2 mg/kg/day by infusion.

What is not established

  • No human parameters

  • No human safety data

  • No human efficacy data

  • No validated dose for any human use

  • Any human microgram figure circulating in community sources is not derived from published clinical evidence

Safety

No human safety data exist. Theoretical risks are as for any IGF-1 analog: hypoglycemia (insulin-like activity), mitogenic effects, and unknown effects of reduced IGFBP binding on growth factor signaling dynamics. Research-grade material identity, purity, and bioactivity are not independently verified for this atlas.

Unknowns and product-quality risks

All safety, , and efficacy parameters are unknown in humans. Gray-market IGF-1 DES may be improperly synthesized, contain truncation variants other than the intended des(1-3), or have unknown degradation profiles.

Interactions and special populations

No data exist.

Regulatory, compounding, and sport notes

Des(1-3) IGF-1 is an IGF-1 analog and falls within prohibition. No authorized human medicinal product was identified in the jurisdictions and regulator databases reviewed; that finding is not a universal legal opinion.

Evidence gaps

  • No human study of any kind published

  • No toxicology or safety pharmacology data

  • No data in humans

  • No regulatory submissions or clinical trial registrations

  • The entire evidence base consists of cell-culture bioassays and rodent studies from the late 1980s and early 1990s

Search notes

  • Databases and registries: PubMed, PubChem, FDA Drugs@FDA

  • Search terms: "des(1-3)IGF-1", "IGF-1 DES", "destripeptide IGF-1", "truncated IGF-1"

  • Last searched: 2026-08-06

  • Inclusion emphasis: Primary peer-reviewed primary data for the specific truncated variant

Sources

  1. Lemmey AB et al. IGF-I and des-(1-3)IGF-I enhance growth in rats after gut resection. Am J Physiol. 1991;260(2 Pt 1):E213-E219. https://pubmed.ncbi.nlm.nih.gov/1996625/

  2. Ballard FJ et al. Des(1-3)IGF-I: a truncated form of IGF-I. Prog Growth Factor Res. 1991;3(1):35-43.

  3. Francis GL et al. Biological activity of des(1-3)IGF-I. J Mol Endocrinol. 1992;8(3):213-223.

  4. WADA Prohibited List 2026. https://www.wada-ama.org/en/prohibited-list

専門家の声

専門家の見解

コメントは個人の見解であり、エビデンスレビューの一部ではありません。掲載は支持を意味しません。

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ビデオ

質問

What is Des(1-3) IGF-1 and how is it different from mecasermin?

Des(1-3) IGF-1 is a 67-amino-acid truncated variant of human IGF-1 missing the N-terminal tripeptide Gly-Pro-Glu. It is explicitly distinct from the FDA-approved drug mecasermin (full-length rhIGF-1). The approval of mecasermin does not apply to this truncated variant.

Is Des(1-3) IGF-1 approved for human use?

No FDA-approved product or EMA-authorized medicine was identified as of 2026-08-06; status elsewhere requires a current national-register check. No human clinical studies have been published.

What evidence exists for Des(1-3) IGF-1 being more potent than regular IGF-1?

In cell assays, Des(1-3) IGF-1 is approximately 7–10 times more potent than native IGF-1, and in rodent models approximately 2.5 times more potent. This enhanced potency reflects reduced IGFBP binding (an availability effect), not stronger receptor affinity. No controlled human trials exist.

What are the safety risks of Des(1-3) IGF-1?

No human safety data exist. Theoretical risks are as for any IGF-1 analog: hypoglycemia due to insulin-like activity, mitogenic effects, and unknown effects of reduced IGFBP binding on growth factor signaling dynamics. Gray-market material may contain truncation variants other than the intended des(1-3).

Is Des(1-3) IGF-1 prohibited by WADA?

Yes. Des(1-3) IGF-1 is an IGF-1 analog and falls within WADA S2 prohibition. No authorized human medicinal product was identified in the jurisdictions and regulator databases reviewed.

Does Des(1-3) IGF-1 occur naturally?

The peptide was first identified in bovine colostrum and human brain tissue as a naturally occurring truncated form of IGF-1. It is distinct from the FDA-approved drug mecasermin (full-length rhIGF-1).

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